2020
Mouse model of SARS-CoV-2 reveals inflammatory role of type I interferon signaling
Israelow B, Song E, Mao T, Lu P, Meir A, Liu F, Alfajaro MM, Wei J, Dong H, Homer RJ, Ring A, Wilen CB, Iwasaki A. Mouse model of SARS-CoV-2 reveals inflammatory role of type I interferon signaling. Journal Of Experimental Medicine 2020, 217: e20201241. PMID: 32750141, PMCID: PMC7401025, DOI: 10.1084/jem.20201241.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin-Converting Enzyme 2AnimalsBetacoronavirusCell Line, TumorCoronavirus InfectionsCOVID-19DependovirusDisease Models, AnimalFemaleHumansInflammationInterferon Type ILungMaleMiceMice, Inbred C57BLMice, TransgenicPandemicsParvoviridae InfectionsPeptidyl-Dipeptidase APneumonia, ViralSARS-CoV-2Signal TransductionVirus ReplicationConceptsSARS-CoV-2Type I interferonMouse modelI interferonRobust SARS-CoV-2 infectionSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2SARS-CoV-2 infectionRespiratory syndrome coronavirus 2SARS-CoV-2 replicationCOVID-19 patientsSyndrome coronavirus 2Patient-derived virusesSignificant fatality ratePathological findingsInflammatory rolePathological responseEnzyme 2Receptor angiotensinFatality rateVaccine developmentGenetic backgroundViral replicationCoronavirus diseaseMice
2014
Hepatitis C virus genetics affects miR-122 requirements and response to miR-122 inhibitors
Israelow B, Mullokandov G, Agudo J, Sourisseau M, Bashir A, Maldonado AY, Dar AC, Brown BD, Evans MJ. Hepatitis C virus genetics affects miR-122 requirements and response to miR-122 inhibitors. Nature Communications 2014, 5: 5408. PMID: 25403145, PMCID: PMC4236719, DOI: 10.1038/ncomms6408.Peer-Reviewed Original ResearchMeSH KeywordsBase SequenceHepacivirusHepatitis CHumansLiverMicroRNAsMolecular Sequence DataPoint MutationVirus ReplicationConceptsMiR-122Hepatitis C virus replicationRecent clinical trialsC virus replicationMiR-122 inhibitionMiR-122 inhibitorClinical trialsHCV replicationMiR-122 knockdownHCV drugsHCV variantsHCVHCV genomeViral titresVirus replicationNext-generation sequencingTransient inhibitionVirus geneticsViral adaptationViral sequencesInhibitionNucleotide changesSingle nucleotide changePatientsTitresHepG2 cells mount an effective antiviral interferon‐lambda based innate immune response to hepatitis C virus infection
Israelow B, Narbus CM, Sourisseau M, Evans MJ. HepG2 cells mount an effective antiviral interferon‐lambda based innate immune response to hepatitis C virus infection. Hepatology 2014, 60: 1170-1179. PMID: 24833036, PMCID: PMC4176518, DOI: 10.1002/hep.27227.Peer-Reviewed Original ResearchConceptsInnate immune responseHCV infectionHuh-7.5 cellsInnate immune systemImmune responseImmune systemAntiviral responseEntire HCV life cycleHepatitis C virus exposurePersistent life-long infectionHepatitis C virus infectionMelanoma differentiation-associated protein 5C virus infectionRobust antiviral responseImportance of IFNHuh-7Retinoic acid-inducible gene IHCV life cycleAcid-inducible gene ILife-long infectionInnate immune antagonistsHepG2 cellsLike receptor pathwayLiver-specific microRNAHCV recognition
2013
Temporal Analysis of Hepatitis C Virus Cell Entry with Occludin Directed Blocking Antibodies
Sourisseau M, Michta ML, Zony C, Israelow B, Hopcraft SE, Narbus CM, Martín A, Evans MJ. Temporal Analysis of Hepatitis C Virus Cell Entry with Occludin Directed Blocking Antibodies. PLOS Pathogens 2013, 9: e1003244. PMID: 23555257, PMCID: PMC3605286, DOI: 10.1371/journal.ppat.1003244.Peer-Reviewed Original ResearchConceptsHCV cell entryHepatitis C virusClaudin-1Complete HCV life cycleCell entryTight junction protein claudin-1HCV life cyclePost-binding stageMiR-122 expressionHepatitis C virus cell entryHepG2 cellsNumerous host factorsVirus cell entryHCV therapyLiver diseaseC virusInfection assaysBlocking antibodiesHCV isolatesSR-BIHost cell entryHost factorsUtilization differencesMajor causeOccludin